scholarly journals Management of Presumed Acute Kidney Injury during Hypertensive Therapy: Stay Calm and Carry on?

2020 ◽  
Vol 51 (2) ◽  
pp. 108-115
Author(s):  
Teresa K. Chen ◽  
Chirag R. Parikh
Keyword(s):  
Blood Pressure ◽  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Blood Pressure Control ◽  
Kidney Injury ◽  
Pressure Control ◽  
Intensive Treatment ◽  
Urinary Biomarkers ◽  
Increased Risk ◽  
Intensive Blood Pressure

Background: Recent studies have demonstrated that intensive blood pressure control is associated with improved cardiovascular outcomes. Acute kidney injury (AKI), however, was more common in the intensive treatment group prompting concern in the nephrology community. Summary: Clinical trials on hypertension control have traditionally defined AKI by changes in serum creatinine. However, serum creatinine has several inherent limitations as a marker of kidney injury, with various factors influencing its production, secretion, and elimination. Urinary biomarkers of kidney injury and repair have the potential to provide insight on the presence and phenotype of kidney injury. In both the Systolic Blood Pressure Intervention Trial and the Action to Control Cardiovascular Risk in Diabetes study, urinary biomarkers have suggested that the increased risk of AKI associated with intensive treatment was due to hemodynamic changes rather than structural kidney injury. As such, clinicians who encounter rises in serum creatinine during intensification of hypertension therapy should “stay calm and carry on.” Alternative explanations for serum creatinine elevation should be considered and addressed if appropriate. When the rise in serum creatinine is limited, particularly if albuminuria is stable or improving, intensive blood pressure control should be continued for its potential long-term benefits. Key Messages: Increases in serum creatinine during intensification of blood pressure control may not necessarily reflect kidney injury. Clinicians should evaluate for other contributing factors before stopping therapy. Urinary biomarkers may address limitations of serum creatinine as a marker of kidney injury.

Impact of Admission Hypertension on Rates of Acute Kidney Injury in Intracerebral Hemorrhage Treated with Intensive Blood Pressure Control

2018 ◽  
Vol 28 (3) ◽  
pp. 344-352 ◽  
Author(s):  
Hannah Hewgley ◽  
Stephen C. Turner ◽  
Joseph E. Vandigo ◽  
Jacob Marler ◽  
Heather Snyder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Acute Kidney Injury ◽  
Intracerebral Hemorrhage ◽  
Blood Pressure Control ◽  
Kidney Injury ◽  
Pressure Control ◽  
Intensive Blood Pressure

scholarly journals A rare case of posterior reversible encephalopathy syndrome in a patient with severe leptospirosis complicated with rhabdomyolysis and acute kidney injury; a case report

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jayawardane Pathiranage Roneesha Lakmali ◽  
Kanapathipillei Thirumavalavan ◽  
Danapala Dissanayake
Keyword(s):  
Blood Pressure ◽  
Acute Kidney Injury ◽  
Blood Pressure Control ◽  
Posterior Reversible Encephalopathy Syndrome ◽  
Vision Loss ◽  
Kidney Injury ◽  
Pressure Control ◽  
Posterior Reversible Encephalopathy ◽  
Peripheral Nerve Involvement ◽  
Reversible Encephalopathy

Abstract Background Leptospirosis is a zoonotic spirochetal disease caused by Leptospira interrogans. The clinical presentation ranges from an asymptomatic state to a fatal multiorgan dysfunction. Neurological manifestations including aseptic meningitis, spinal cord and peripheral nerve involvement, cranial neuropathies and cerebellar syndrome are well recognized with varying frequencies among patients with this disease. Posterior reversible encephalopathy syndrome is a very rare occurrence in leptospirosis and only two cases are reported in the medical literature up to now. We report a case of posterior reversible encephalopathy syndrome in a patient with leptospirosis with rhabdomyolysis and acute kidney injury. Case presentation A 21 year-old male presented with fever and oliguric acute kidney injury with rhabdomyolysis. A diagnosis of leptospirosis was made and he was being managed according to the standard practice together with regular hemodialysis. The clinical condition was improving gradually. On day 8 of the illness, he developed headache and sudden painless complete bilateral vision loss followed by several brief generalized tonic clonic seizure attacks. Examination was significant for a Glasgow Coma Scale of 14/15, blood pressure of 150/90 mmHg and complete bilateral blindness. The findings of magnetic resonance imaging of the brain were compatible with posterior reversible encephalopathy syndrome. He was managed with blood pressure control and antiepileptics with supportive measures and standard treatment for leptospirosis and made a complete recovery. Conclusion Posterior reversible encephalopathy syndrome, though very rare with leptospirosis, should be considered as a differential diagnosis in a patient with new onset visual symptoms and seizures, especially during the immune phase. Optimal supportive care together with careful blood pressure control and seizure management would yield a favourable outcome in this reversible entity.

Acute Kidney Injury following Cardiac Surgery: Role of Perioperative Blood Pressure Control

2011 ◽  
Vol 33 (5) ◽  
pp. 438-452 ◽  
Author(s):  
Matthew R. Weir ◽  
Solomon Aronson ◽  
Edwin G. Avery ◽  
Charles V. Pollack, Jr.
Keyword(s):  
Blood Pressure ◽  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Blood Pressure Control ◽  
Kidney Injury ◽  
Pressure Control

scholarly journals Are We Barking Up the Wrong Tree? Rise in Serum Creatinine and Heart Failure

2019 ◽  
Vol 48 (3) ◽  
pp. 193-195
Author(s):  
Amir Kazory ◽  
Claudio Ronco
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Serum Creatinine ◽  
Renal Injury ◽  
Kidney Injury ◽  
Pressure Control ◽  
Adverse Outcomes ◽  
Patients With Heart Failure ◽  
Severe Hyperkalemia ◽  
Intensive Blood Pressure

A significant subset of patients with heart failure (HF) experience small to moderate rise in serum creatinine (RSC) in the setting of otherwise beneficial therapies such as aggressive diuresis or renin-angiotensin-aldosterone system (RAAS) inhibition. Accumulating data suggest that RSC in this setting is dissimilar from conventional causes of renal insult in that it has a negligible impact on the outcomes. There is also emerging evidence on the lack of association between biomarkers of renal injury and RSC in the setting of aggressive diuresis. A similar pattern has been observed in recent hypertension trials where the RSC in patients with intensive blood pressure control has not been associated with biomarker evidence of renal injury or adverse outcomes. Based on these findings, RSC, rather than acute kidney injury, appears to be the preferred terminology in HF (and possibly in hypertension) because of its purely descriptive nature that lacks any potentially inaccurate implication of mechanistic or prognostic reference. From a pragmatic viewpoint, we believe that small to moderate RSC is to be anticipated and tolerated with RAAS inhibition and/or aggressive diuresis in acute or chronic HF and should not prompt discontinuation of the therapy unless complications such as hypotension and severe hyperkalemia develop.

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